BC002059/ABHD10 轴调控的 miR-19b-3p 促进心肌梗死细胞凋亡。
MiR-19b-3p regulated by BC002059/ABHD10 axis promotes cell apoptosis in myocardial infarction.
机构信息
Department of Cardiology, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China.
Department of Gastroenterology, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, 1017 Dongmen North Road, Luohu District, Shenzhen, 518000, Guangdong, China.
出版信息
Biol Direct. 2022 Aug 18;17(1):20. doi: 10.1186/s13062-022-00333-x.
BACKGROUND
Recently, microRNAs (miRNAs), have been extensively investigated in diseases. The upregulated expression of miR-19b-3p has been validated in patients with hypertrophic cardiomyopathy. Nonetheless, it regulatory mechanism in myocardial infarction (MI) is still unclear.
PURPOSE
This research aimed to investigate the role and molecular regulation mechanism of miR-19b-3p in MI.
METHODS
QRT-PCR and western blot assays measured RNA and protein expression. Cell apoptosis were tested by flow cytometry and TUNEL assays. Cell viability was measured by trypan blue staining method. RIP and luciferase report assays examined gene interaction. The assays were performed under hypoxia condition.
RESULTS
MiR-19b-3p was highly expressed in myocardial cell line H9C2, primary cardiomyocytes, and tissues from MI mouse model. MiR-19b-3p inhibition suppressed the apoptosis of cardiomyocytes. BC002059 could up-regulate ABHD10 through sequestering miR-19b-3p. BC002059 upregulation was observed to repress cell apoptosis. Rescue experiments demonstrated that miR-19b-3p overexpression abrogated the suppressive impact of BC002059 on the apoptosis of MI cells, and infarct size, area at risk as well as CK-MB and LDH release of MI mouse model tissues, which was further abolished via ABHD10 increment.
CONCLUSION
MiR-19b-3p regulated by BC002059/ABHD10 axis promotes cell apoptosis in MI, which might provide a novel perspective for MI alleviation research.
背景
最近，microRNAs（miRNAs）在疾病中的研究已经广泛开展。miR-19b-3p 的上调表达已在肥厚型心肌病患者中得到验证。然而，其在心肌梗死（MI）中的调控机制尚不清楚。
目的
本研究旨在探讨 miR-19b-3p 在 MI 中的作用和分子调控机制。
方法
实时荧光定量 PCR（QRT-PCR）和 Western blot 检测 RNA 和蛋白表达。通过流式细胞术和 TUNEL 检测细胞凋亡。通过台盼蓝染色法检测细胞活力。RIP 和荧光素酶报告基因检测实验研究基因相互作用。所有实验均在缺氧条件下进行。
结果
miR-19b-3p 在心肌细胞系 H9C2、原代心肌细胞和 MI 小鼠模型组织中高表达。miR-19b-3p 抑制可抑制心肌细胞凋亡。BC002059 可通过结合 miR-19b-3p 上调 ABHD10。BC002059 的上调观察到可抑制细胞凋亡。挽救实验表明，miR-19b-3p 的过表达可消除 BC002059 对 MI 细胞凋亡的抑制作用，以及 MI 小鼠模型组织中梗死面积、危险区面积以及 CK-MB 和 LDH 释放的作用，通过增加 ABHD10 进一步消除。
结论
BC002059/ABHD10 轴调控的 miR-19b-3p 促进 MI 中的细胞凋亡，这可能为 MI 缓解研究提供新的视角。
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